Cardiogenic and other shocks in a glance

Shock is the failure of the cardiovascular system to  provide adequate blood flow to organs and tissues . it also has been defined as a reduction of cardiac output or a poor distribution of output to a point where potentially irreversible tissue damage occurs .

Pathophysiologic classification shock

Blood flow is determined by three entities : Blood volume , vascular resistance , and pump function. Thus , there are three types of shock : Hypovolemic , vasogenic and cardiogenic . example of causes of hypovolemic shock are gastrointestinal bleeds , ruptured aortic aneurysm , and sever diabetic ketoacidosis . examples of  vasogenic shock include septic shock , anaphylactic shock , neurogenic shock and shock from pharmacologic causes . there was a wide variety  of causes of Cardiogenic shock , although acute myocardial infarction is the most common . pulmonary embolism can classified separately as obstructive but ahs a presentation similar to cardiogenic shock .


Stages of Shock

Stage I: Hypotension compensated.

Hypotension may be due to decreased cardiac output or vasodilation. The initial event in the great majority of cases of Shock is a fall in cardiac output rather than vasodilation.

The fall in minute volume and hypotension set in motion compensatory mechanisms, which improve the low blood pressure and maintain traffic flow of vital organs like the heart and brain.

Stage II: Decreased perfusion tissue.      

Compensatory mechanisms to maintain perfusion of vital organs are functioning at its peak, but still insufficient.

The renal hypoperfusion reduces urine output volume, and subjects with coronary diseases signs of ischemia. The external condition of the patient shows marked sympathetic activity, with excess production of catechols skin with cyanosis, cold sweats and clammy, and poor skin perfusion.

Stage III: failure of the microcirculation with cellular injury.

The excessive and prolonged reduction of tissue perfusion produces a significant alteration in the function of cell membranes, aggregation of blood cells with marked circulatory disturbance in capillary flow, marked decrease in blood flow induce cell damage. Blood pressure gradually falls to critical levels at which they assume at perfución renal organ leads to the installation of an acute tubular necrosis.

The gastrointestinal tract ischemia produces necrosis of the intestinal epithelium to absorb bacteria and toxic products that damage the other vascular endothelium causing a syndrome of disseminated intravascular coagulation.

Severe metabolic acidosis resulting from anaerobic metabolism, further worsening the state of hypotension, this hypotension reduces coronary artery perfusion, especially in those patients with coronary artery disease.

This hyperfusion tissue cause cellular damage sustained.

The capillary endothelial injury leads to loss of fluids and proteins into the extravascular behavior exacerbating hypovolemia and hypotension. The cell membrane injury by ischemia and acidosis occurs with disruption of lysosomes loss of enzymes, alteration of the sodium pump with ionic imbalance, reduction and then loss of energy reserves – dependent, thus reaching to cell death.

Signs which are helpful in classifying shock ?

The patient’s history will usually make the diagnosis , but patients may present with shock of undetermined etiology . the clinician mist then rely on the clinical examinations to classify the shock state . feeling the extremities and examining the jugular veins provide vital clues . warm skin is suggestive of a vasogenic cause ; cool , clammy skin reflects enhanced reflex sympathoadrenal discharge leading to cutaneous vasoconstriction , suggesting hypovolemic or cardiogenic shock . distended jugular veins. Rales , or an S3 gallop suggest a cardiogenic cause rather than hypovolemic . measured central venous pressure may aid in differentiating hypovolemic from cardiogenic shock . subclavian vein cannulation should be avoided if a myocardial infarction is suspected , as thrombolytic agents may be needed .

10 causes of cardiogenic shock

1-      Acute MI( the most common cause )

2-      Acute myocarditis

3-      Chronically congestive cardiomyopathy

4-      Valvular heart disease

5-      Myocardial contusion

6-      Arrhythmias

7-      Toxin , drugs

8-      Hypothermia

9-      Hyperthermia

10-  Left atrial myxoma

What are the classic changes in systemic vascular resistance and cardiac output in septic shock ?

In classic “warm”septic shock , the systemic vascular resistance is reduced and cardiac output is increased . the increase in cardiac output is a compensatory mechanism for the decrease in vascular resistance . it is not completely compensatory because of a circulating myocardial depressant factor ; released in sepsis . the identity of this factor has not yet been agreed upon .

How can septic shock appear like cardiogenic shock ?

In hypodynamic or “cold”septic shock , seen more frequently in the elderly , there are two causes for reduced cardiac output . first , the myocardial depressant factor decreases the cardiac index . second , in progressive sepsis , there are increases in pulmonary capillary resistance . these factors cause a significant decrease in cardiac output and present clinically like right-sided congestive heart failure . cold septic shock has a very high mortality .

Killip classification of pump dysfunction in acute myocardial infarction .

The killip classification is based on clinical criteria that correlate the degree of pump dysfunction with acute mortality in patients with myocardial infarction .

Calss I: has no evidence of left ventricular failure and has a 5% mortality .

ClassII: has bibasilar rate , an s3 gallop or heart failure by chest x-ray and a 15-20% mortality .

Class III: patients are in pulmonary edema . these patients have a 40% mortality .

Calss IV:  patients are in cardiogenic shock defied by : (1) systolic blood pressure <90mmHg. (2) peripheral vasoconstriction ,(3) ologuria and , (4) pulmonary vascular congestion . class IV patients have a mortality of 80% .

Significance of loud holosystolic murmur in a patient with shock and an acute myocardial infarction

Loud holosystolic murmur with myocardial infarction indicates either papillary muscle rupture or an acute ventricular septal defect(VSD) .  these may be indistinguishable , but acute VSD usually occurs with an anteroseptal myocardial infarction and has an associated palpable thrill . and is usually seen in inferior myocardial infarctions. These frequently cause shock on the basis of much reduced forward blood flow and can be differentiated by echocardiography or Swan-Ganz catheterization . Both reqire emergent cardiothoracic surgery for early repair. In some patients, the murmur may be soft or inaudible .

Massive pulmonary embolism Vs. shock

Massive pulmonary embolism causes shock on the basis of reduced  cross- sectional area of the pulmonary tract . shock occurs when the cross-sectional area is reduced  by 50% or more . In an acute situation . the right ventricle can increase its systolic pressure only to a maximum of about 40 mmHg . this pressure is inadequate to overcome the increased resistance , blood flow is reduced and shock develops . massive pulmonary embolism presents with the following sign and symptom .













Chest pain


Systolic BP <80mmHg



Cardiac arrest


Emergency treatment of cardiogenic shock

Supplemental oxygen should be provided . arrhythmias should be treated by protocols specified in the American’s heart association textbook of (ACLS) . if the patient is not in pulmonary edema , volume can be administered in a aliquots of 200-300 ml of crystalloid . This is particularly true in inferior myocardial or if there is electrocardiographic evidence of right ventricular infarction . dopamine and dobutamine are the pressors of choice for improvement of hemodynamics . dobutamine is likely to be a better choice , particularly if there is evidence of pulmonary edema , since dobutamine unlike dopamine , reduces left ventricular-end-diastolic pressure . emergency angioplasty may improve survival in patients with cardiogenic shock from myocardial infarction .

Therapeutic measures may improve shock from a pulmonary embolism

Massive pulmonary embolism should be treated similarly to cardiogenic shock from myocardial infarction : oxygen ( intubation if necessary ) , volume , and pressors . thrombolytics have not been studies well enough in massive pulmonary embolism to show improved survival . however, the use of tissue plasminogen activator , streptokinase and urokinase has been demonstrated to  improve hemodynamics with reduced tricuspid regurgitation , reduced right ventricular dilatation , and imprived cardiac output in patients with massive pulmonary embolism , and thus the use of thrombolytics should be considered . emergency embolectomy can also be considered .

Cause of traumatic cardiogenic shock

Pericardial Tamponade , myocardial contusion , tension peneumothorax , and air embolism from bronchial tears .

Acute pericardial Tamponade occurs in about 2 % of penetrating chest trauma cases and is more common with stab wounds than gunshot wounds . Tamponade is rare after blunt trauma . Beck;s classic traid of distended neck veins , decreases arterial pressure , and muffled heart sound occurs onl in about a third of patients . A high central venous pressure with tachycardia and hypotension in penetrating trauma are reliable sign of Tamponade. Examination and chest radiography will exclude tension pneumothorax .

Does CPR resuscitate patients in cardiac arrest ?

Cardiopulmonray resuscitation (CPR) rarely resuscitates patients from cardiac arrest without early institution of advanced life support interventions : defibrillation, airway management , and administration of appropriate drugs . all cardiac arrest victims should have a monitor placed as soon as possible , as immediate defibrillation is indicated in patients in ventricular fibrillation .

Two mechanism have been proposed to explain blood flow with closed chest compression . the thoracic pump theory suggests that the heart acts as the passive conduit , with systolic and mean arterial pressure and blood flow to the carotid artery augmented by increased thoracic pressure . Intrathoracic pressure is transmitted into the extrathoracic arteries to a greater extent than into the extrathoracic veins . this is reflected in an extrathoracic arterial – venous pressure gradient . the unequal transmission of intrathoracic pressure into the extrathoravic arteries and veins results from the presence of venous valves and unequal arterial and venous capacitance and collapsibility . arteries resist collapse and therefore transmit the intrathoracic pressure into the extrathoracic arterial bed .

The cardiac theory suggests that the heart itself is compressed , creating a pressure gradient between intracardiac and extracardiac structures . however . there are not enough data at present to determine which mechanism predominates .

Reversible common causes of cardiac arrest and their specific treatment

Cardiac arrest may be successfully resuscitated in a number of cases if the underlying etiology is recognized and promptly treated .

1-      Ventricular fibrillation and ventricular tachycardia . immediate defibrillation should be performed before other procedure , as the success rate decreases by 4% with every minute of delay .

2-      Tension pneumothorax : this condition should be suspected  following positive pressure ventilation in a cardiac arrest patient who has a decrease in breath sounds on the affected side . subcutaneous air or resistance to airflow with bagging . the treatment is needle decompression at the fifth intercostal space , followed by thoracotomy .

3-      Hyperkalemia . heralded by wide QRS complexes and the absence of P waves, hyperkalemia should be suspected as the cause of arrest in patient s with renal failure . calcium chloride should be administered immediately , followed by sodium bicarbonate and an insulin –glucose drip .

4-      Anaphylaxis . this should be suspected whenever cardiac arrest occurs following administration of parenteral medications . As asphyxia or shock is the underlying mechanism, aggressive intervention with endotracheal intubation , fluid and intravenous epinephrine should be performed immediately .

IV calcium in cardiac arrested patients

Overall patients in cardiac arrest do not appear to benefit from the use of intravenous calcium . Indications are thus limited to three specific causes of cardiac arrest : hyperkalemia , hypocalcemia , and possibly calcium antagonist overdose . calcium chloride should be administered at a dose of 2-4 mg/kg of a 10% solution intravenously every 10 minutes .

Neurologic outcome prediction following successful resuscitation of cardiac arrest

Several reports have attempted to develop prognostic signs for cerebral recovery following CPR . the duration of coma is the most reliable prognostic sign . however, recovery of consciousness has occurred after 10 days of coma . reactive pupils, oculocephalic reflexes , spontaneous respirations and purposeful response to paiful stimuli are associated with a higher percentage of neurologic recovery . however, a favorable outcome may rarely occur in patients with poor prognostic sign .

About Dr.Nabil Paktin

Cardiologist , M.D.,F.A.C.C.

Posted on March 27, 2013, in Uncategorized. Bookmark the permalink. Leave a comment.

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